Histone deacetylases (HDACs) play a role in the reversible acetylation of histones, transcription factors, and other proteins, which are associated with chromatin remodeling and regulation of gene expression. Acute myeloid leukemia (AML) arises, in part, from disordered hematopoiesis as a consequence of multiple cooperative mutations or alternations disrupting differentiation, proliferation and survival programs in hematopoietic progenitors. Recurrent chromosomal abnormalities in AML frequently involve transcription factor fusion proteins that contribute to unique etiology and prognosis (1). Chromosomal 16 inversion, inv(16)(p13.1q22) or t(16;16)(p13.1;q22) is found in approximately 5-12% of AML patients and is associated with dismal prognosis. Accordingly, new treatments for AML patients are necessary. Provided herein are solutions to these and other problems in the art.